The purpose of the proposed study is to investigate effects of pulmonary interstitial edema on (1) lung surfactant, and its role in promoting alveolar flooding and on (2) interstitial pressure, with particular emphasis on the interactions between this pressure and lung elastic recoil. It is hypothesized that as interstitial swelling progresses to the point where fluid leakage into the alveolar subphase is initiated, surfactant stability diminishes and the resultant higher mean surface tension further increases the rate of fluid transudation. This mechanism would help to account for some of the loss of compliance occurring in interstitial edema. It would also contribute to the rapid flooding seen at the critical stages of lung edema. Experiments are designed to test this hypothesis, some of which will utilize micropressure measurements in the subphase and interstitium. A model of interstitial mechanics is proposed in which the fluid pressure in normal lung is negative, and becomes more negative when alveolar walls are stretched during lung inflation. This could contribute appreciably to the increase in lung retractive force seen during inflation. When the interstitial space swells, these negative pressure relationships should be altered. Additional experiments are designed to investigate these predictions and to develop a more thorough understanding of the mechanics of the interstitium.